MCRC Principal Investigators

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Richard Karas, M.D., Ph.D.

Dr. Karas received his undergraduate degree in Earth and Planetary Sciences from Johns Hopkins University in 1978, his Ph.D. in Biology from Harvard University in 1984, and his M.D. degree from Tufts University in 1986. He then did his residency in Internal Medicine at Brigham and Women's Hospital followed by a clinical cardiology fellowship at Duke University and a research fellowship at the University of Texas, Southwestern Medical Center in Dallas. Dr. Karas, the Elisa Kent Mendelsohn Professor of Molecular Cardiology and Medicine at Tufts University School of Medicine, is the Chief Scientific Officer of Tufts Medical Center, the Executive Director of the Molecular Cardiology Research Institute and Director of the MCRC. In addition, Dr. Karas is Vice Chairman for Scientific Affairs for the Department of Medicine, Director of Preventive Cardiology and Co-Director of the Women's Heart Center at Tufts Medical Center.

Research Interests

Dr. Karas' major research interest is the effect of estrogen on the cardiovascular system. More specifically, Dr. Karas' research focuses on the molecular pathways that mediate estrogen's direct effects on vascular cells. Recent studies from the MCRC have shown that estrogen receptors in vascular cells can be activated in several novel ways, and several of these signaling pathways are actively being studied in the lab. Current studies are directed at understanding the role of rapid estrogen receptor signaling, and how this shares cross-talk with traditional genomic signaling pathways. Estrogens effects on microRNA expression are also being studied. Ongoing, as well, are attempts to clone novel estrogen receptor-interacting proteins that regulate receptor activation. In addition to these cell-based, molecular studies, Dr. Karas also uses whole animal, mouse models of cardiovascular diseases to study the effects of estrogen on the vascular system in vivo. In conjunction with the MCRI's mouse physiology core and mouse transgenic core laboratories, studies of estrogens effects on the response to vascular injury, on myocardial infarction, and on cardiac electrophysiology are all ongoing. These studies take advantage of the availability of several different genetically altered mouse models to define the molecular pathways that mediate estrogens effects. Finally, Dr. Karas also maintains an active interest in clinically-based studies focused on the regulation of vasomotor tone and on the effects of lipid lowering interventions and adverse events related to lipid-altering interventions.

Richard Karas

Pilar Alcaide, Ph.D.

Dr. Alcaide received her PhD in Molecular Biology from Universidad Autonoma of Madrid, Spain, where she studied the immunological aspects Trypanosoma cruzi infection, the protozoan parasite that causes Chagas disease. As a recipient of a Fulbright postdoctoral fellowship, Dr. Alcaide trained in Dr. F.W Luscinskas laboratory in the Center for Excellence in Vascular Biology at the Brigham and Women’s hospital where she trained in vascular biology and studied how different types of leukocytes are recruited into tissues during the immune response, as well as how junctional molecules expressed in endothelial cells can actively regulate the passage of leukocytes, which is a critical process during inflammation. After completion of her postdoctoral research training, Dr. Alcaide was appointed to Instructor of Pathology at Harvard Medical School and two years later joined the faculty at MCRI. The Alcaide lab combines the areas of immunology and vascular biology to study several aspects of recruitment of T lymphocytes in diverse inflammatory settings based on their interactions with the activating endothelium. The over-arching goal in the lab is to better understand the processes that take place during T lymphocyte recruitment in both the immune cells and the activated endothelium, and how those can potentially be targeted in therapeutically useful ways. We are particularly interested in understanding how Th 17 cells, a highly inflammatory T cell type, differ from other T cell subsets and leukocytes in their interactions with endothelial cells and during migration to inflammatory sites. The lab combines in vitro flow systems and videomicroscopy to study leukocyte-endothelial cell interactions, and several in vivo mouse models of inflammation.

Pilar Alcaide

Robert Blanton, M.D.

Originally from Texas, Rob attended college and medical school at Washington University in St. Louis. He joined the MCRI and the Cardiology Division in 2005 as a clinical/research fellow, following his residency training in internal medicine at Barnes-Jewish Hospital. He completed his cardiovascular fellowship in 2009 and is now an Assistant Professor of Medicine. Rob's research examines the molecular mechanisms regulating the development and inhibition of cardiac hypertrophy. In addition, he serves as the Scientific Director of the MCRI Mouse Physiology Core.

Robert Blanton

Navin Kapur, M.D.

Navin Kumar Kapur is an Assistant Professor of Medicine at Tufts University School of Medicine and a staff member of the Division of Cardiology at Tufts Medical Center. Dr. Kapur received his M.D. from Georgetown University in Washington D.C. He completed training as a medical resident at Beth Israel Deaconess Medical Center followed by fellowships in Adult Cardiology, Heart Failure, and Interventional Cardiology at Johns Hopkins Hospital in Baltimore, MD. As part of an NIH Training Grant directed by Dr. David Kass, Dr. Kapur completed his postdoctoral research training in the laboratory of Dr. Jeffrey Rade at Johns Hopkins. During this time, Dr. Kapur explored the paracrine effects of transforming growth factor-beta (TGFb) on endocardial thromboresistance in heart failure.

The Kapur laboratory is studying the role of endoglin, a TGFb co-receptor, in cardiac fibrosis. The lab uses molecular approaches to study endoglin’s effect on extracellular matrix synthesis in human cardiac fibroblasts and employs animal models to study the role of endoglin in heart failure and myocardial infarction. As an interventional cardiologist, Dr. Kapur has several clinical studies evaluating the role of soluble endoglin in heart failure and acute myocardial infarction.

Navin Kapur

Iris Jaffe, M.D., Ph.D.

Iris Zamir Jaffe is an Associate Professor of Medicine at Tufts University School of Medicine and a staff member of the Division of Cardiology at Tufts Medical Center. Dr. Jaffe is the co-Director of the MCRC and the Chair of the Department of Medicine's Women in Medicine Committee. She received her M.D. and Ph.D. in Molecular Biology from the University of Pennsylvania in Philadelphia. She did her Ph.D. research in the laboratory of Dr. Mitchell Lazar where she studied the mechanism of transcriptional repression by nuclear hormone receptors. She trained as a medical resident at the Massachusetts General Hospital followed by a fellowship in Cardiology at Brigham and Women's Hospital. Iris completed her postdoctoral training in the laboratory of Michael Mendelsohn within the MCRI.

The Jaffe laboratory is studying the role of vascular mineralocorticoid receptors (MR) in vascular cell function and disease. The lab uses molecular approaches to study the mechanisms of gene regulation by MR in human vascular cells and employs animal models to study the role of MR in vascular dysfunction and atherosclerosis.

Iris Jaffe

Michael Mendelsohn, M.D.

Michael E. Mendelsohn, M.D., F.A.C.C., is currently a Professor of Medicine and member of the Molecular Cardiology Research Institute at Tufts Medical Center. Dr. Mendelsohn founded the MCRI in 1998, and served as its Executive Director from its inception until 2010. Dr. Mendelsohn was also the first recipient of the Elisa Kent Mendelsohn Professorship of Molecular Cardiology and Medicine at Tufts University School of Medicine. On June 1, 2010, Dr. Mendelsohn joined Merck & Co. as Senior Vice President and Head of Cardiovascular Research.

Dr. Mendelsohn is an international leader in the study of molecular vascular biology. As a physician-scientist, Mendelsohn has focused on signal transduction pathways regulating vascular tone and function. His laboratory has contributed importantly to deciphering the mechanisms of action of endogenous vascular protective molecules, including estrogen/estrogen receptors and nitric oxide/cyclic GMP signaling pathways in cardiovascular physiology and disease. Dr. Mendelsohn received his B.A. Magna Cum Laude from Amherst College and his M.D. from Harvard Medical School, followed by residency in Internal Medicine and fellowship in Cardiovascular Medicine at the Brigham and Women's Hospital. He was a member of the staff of the BWH Cardiology Division from 1988-1993 and an Assistant Professor of Medicine at Harvard Medical School. Dr. Mendelsohn’s laboratory is funded principally by the National Institutes of Health. He has been the Principal Investigator on numerous NIH awards, including a Specialized Center of Research in Ischemic Heart Disease and a Program Project Grant studying molecular mechanisms of vascular relaxation. Dr. Mendelsohn’s awards also include election to the American Society of Clinical Investigation (ASCI), the Association of University Cardiologists (AUC) and the Association of American Physicians (AAP).

Michael Mendelsohn

Gavin Schnitzler, Ph.D.

Dr. Schnitzler is an Assistant Professor in Medicine at Tufts University School of Medicine and an Investigator in the Molecular Cardiology Research Institute. Dr. Schnitzler received a B.A. in Biochemistry and in Psychology from Swarthmore College in 1987, and a Ph.D. in Biology from U.C. San Diego in 1993. Dr. Schnitzler completed his post-doctoral training, as a Helen Hay Whitney fellow in the laboratory of Dr. Robert Kingston at Mass. General Hospital/Harvard Medical School, in 1999. Dr. Schnitzler began his independent studies in the Biochemistry Department at TUSM, and moved to the MCRI in 2009.

Dr. Schnitzler's laboratory is studying the roles of chromatin changes in the regulation of transcription by nuclear hormone receptors, including Estrogen Receptor and Glucocorticoid Receptor. The lab uses a combination of standard and high-throughput techniques to understand how the genetic and epigenetic factors that modulate chromatin structure give rise to tissue-specific transcriptional responses to glucocorticoids or estrogen.

Gavin Schnitzler